Parawixin2 Protects Hippocampal Cells in Experimental Temporal Lobe Epilepsy

Autor: Norberto Peporine Lopes, José Luiz Liberato, Wagner Ferreira dos Santos, Andréia Cristina Karklin Fontana, Márcia Renata Mortari, Lívea Dornela Godoy, Rene Oliveira Beleboni, Alexandra Olimpio Siqueira Cunha
Jazyk: angličtina
Rok vydání: 2018
Předmět:
0301 basic medicine
Male
Parawixia bistriata
Health
Toxicology and Mutagenesis

medicine.medical_treatment
spider toxin
Spider Venoms
lcsh:Medicine
Toxicology
Hippocampus
chemistry.chemical_compound
Epilepsy
0302 clinical medicine
pilocarpine model
Urea
Neurons
temporal lobe epilepsy
Riluzole
Neuroprotective Agents
Neuroprotective Agents/therapeutic use
GABAergic
neuroprotection
medicine.symptom
GABA uptake inhibitor
medicine.drug
Parawixin2
Status epilepticus
Neuroprotection
Article
03 medical and health sciences
medicine
Nipecotic acid
Animals
Hippocampus/drug effects
Rats
Wistar

Hippocampal sclerosis
business.industry
lcsh:R
medicine.disease
Spider Venoms/therapeutic use
Urea/analogs & derivatives
Neurons/drug effects
Epilepsy
Temporal Lobe/drug therapy

VENENOS DE ORIGEM ANIMAL
Disease Models
Animal

030104 developmental biology
Anticonvulsant
Epilepsy
Temporal Lobe

chemistry
nervous system
hippocampal lost cells
business
Neuroscience
030217 neurology & neurosurgery
Zdroj: Liberato, J L, Godoy, L D, Cunha, A O S, Mortari, M R, de Oliveira Beleboni, R, Fontana, A C K, Lopes, N P & Dos Santos, W F 2018, ' Parawixin2 Protects Hippocampal Cells in Experimental Temporal Lobe Epilepsy ', Toxins, vol. 10, no. 12 . https://doi.org/10.3390/toxins10120486
Toxins
Volume 10
Issue 12
Toxins, Vol 10, Iss 12, p 486 (2018)
Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual)
Universidade de São Paulo (USP)
instacron:USP
DOI: 10.3390/toxins10120486
Popis: Epilepsy is considered as one of the major disabling neuropathologies. Almost one third of adult patients with temporal lobe epilepsy (TLE) do not respond to current antiepileptic drugs (AEDs). Additionally, most AEDs do not have neuroprotective effects against the inherent neurodegenerative process underlying the hippocampal sclerosis on TLE. Dysfunctions in the GABAergic neurotransmission may contribute not only to the onset of epileptic activity but also constitute an important system for therapeutic approaches. Therefore, molecules that enhance GABA inhibitory effects could open novel avenues for the understanding of epileptic plasticity and for drug development. Parawixin2, a compound isolated from Parawixia bistriata spider venom, inhibits both GABA and glycine uptake and has an anticonvulsant effect against a wide range of chemoconvulsants. The neuroprotective potential of Parawixin2 was analyzed in a model of TLE induced by a long-lasting Status Epilepticus (SE), and its efficiency was compared to well-known neuroprotective drugs, such as riluzole and nipecotic acid. Neuroprotection was assessed through histological markers for cell density (Nissl), astrocytic reactivity (GFAP) and cell death labeling (TUNEL), which were performed 24 h and 72 h after SE. Parawixin2 treatment resulted in neuroprotective effects in a dose dependent manner at 24 h and 72 h after SE, as well as reduced reactive astrocytes and apoptotic cell death. Based on these findings, Parawixin2 has a great potential to be used as a tool for neuroscience research and as a probe to the development of novel GABAergic neuroprotective agents.
Databáze: OpenAIRE